摘要
趋化因子受体最早是在研究白细胞迁移过程中发现的,它在大鼠和小鼠的背根神经节外周感觉神经细胞上也有表达.在炎症情况下,激活的趋化因子受体可以诱导神经细胞上一类重要的镇痛受体———μ-鸦片受体的异源性脱敏,抑制其功能;同时,激活的趋化因子受体还可以增强一类对于痛觉感受非常关键的受体———辣椒素受体的敏感性,使其敏化.趋化因子受体诱导的这2种效应可以通过Gi蛋白信号传导通路增强生物体对痛觉的敏感度.这些结果提示,趋化因子受体可能是免疫系统和神经系统之间交叉调节的桥梁.
Chemokine receptors, originally peripheral sensory neurons in the dorsal root discovered to mediate leukoeytes trafficking, were detected on ganglia of rats and mice. Upon activation, these receptors mediate chemokine-induced heterologous desensitization of μ-opioid receptors, a class of key analgesic receptors on neurons. Furthermore, chemokine treatment also enhances the sensitivity of transient receptor potential vanilloid 1 （TRPV1）, a heat- and ligand-gated calcium channel that is critical for sensing pain. During inflammation, activation of chemokine receptors on neurons contributes to hyperalgesia by inhibiting μ-opioid receptors and concomitantly sensitizing TRPVI, via Gi-protein mediated signaling pathways. Thus, based on above analysis, we proposed that chemokine receptors may serve as a linkage between the immune and neural systems.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2006年第2期101-105,共5页
Chinese Journal of Biochemistry and Molecular Biology
基金
国家自然科学基金资助项目(No.30400401)~~
